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タイトル: Loss of periostin ameliorates adipose tissue inflammation and fibrosis in vivo
著者: Nakazeki, Fumiko
Nishiga, Masataka
Horie, Takahiro  kyouindb  KAKEN_id
Nishi, Hitoo
Nakashima, Yasuhiro  kyouindb  KAKEN_id
Baba, Osamu  kyouindb  KAKEN_id
Kuwabara, Yasuhide
Nishino, Tomohiro
Nakao, Tetsushi
Ide, Yuya
Koyama, Satoshi
Kimura, Masahiro
Tsuji, Shuhei
Sowa, Naoya
Yoshida, Shigeo
Conway, Simon J.
Yanagita, Motoko  kyouindb  KAKEN_id
Kimura, Takeshi  KAKEN_id
Ono, Koh
著者名の別形: 西賀, 雅隆
堀江, 貴裕
西, 仁勇
中島, 康弘
馬場, 理
桑原, 康秀
西野, 共達
中尾, 哲史
井手, 裕也
小山, 智史
柳田, 素子
木村, 剛
尾野, 亘
発行日: 4-Jul-2018
出版者: Springer Nature
誌名: Scientific reports
巻: 8
論文番号: 8553
抄録: Recent evidence suggests that the accumulation of macrophages as a result of obesity-induced adipose tissue hypoxia is crucial for the regulation of tissue fibrosis, but the molecular mechanisms underlying adipose tissue fibrosis are still unknown. In this study, we revealed that periostin (Postn) is produced at extraordinary levels by adipose tissue after feeding with a high-fat diet (HFD). Postn was secreted at least from macrophages in visceral adipose tissue during the development of obesity, possibly due to hypoxia. Postn⁻/⁻ mice had lower levels of crown-like structure formation and fibrosis in adipose tissue and were protected from liver steatosis. These mice also showed amelioration in systemic insulin resistance compared with HFD-fed WT littermates. Mice deficient in Postn in their hematopoietic compartment also had lower levels of inflammation in adipose tissue, in parallel with a reduction in ectopic lipid accumulation compared with the controls. Our data indicated that the regulation of Postn in visceral fat could be beneficial for the maintenance of healthy adipose tissue in obesity.
著作権等: © The Author(s) 2018. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
URI: http://hdl.handle.net/2433/234184
DOI(出版社版): 10.1038/s41598-018-27009-9
PubMed ID: 29867212
出現コレクション:学術雑誌掲載論文等

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